Details

Autor(en) / Beteiligte

• Wang, Xuan
• Zhu, Yan-Bin
• Cui, Hai-Peng
• Yu, Ting-Ting

Titel

Aberrant promoter methylation of p15INK4b and p16INK4a genes may contribute to the pathogenesis of multiple myeloma: a meta-analysis

Ist Teil von

• Tumor biology, 2014, Vol.35 (9), p.9035-9043

Ort / Verlag

Dordrecht: Springer Netherlands

Erscheinungsjahr

2014

Link zum Volltext

Quelle

SpringerLink (Online service)

Beschreibungen/Notizen

• We carried out the current meta-analysis aiming to comprehensively assess the potential role of p15 INK4b and p16 INK4a aberrant promoter methylation in the pathogenesis of multiple myeloma (MM). The MEDLINE (1966 ~ 2013), Cochrane Library (Issue 12, 2013), EMBASE (1980 ~ 2013), CINAHL (1982 ~ 2013), Web of Science (1945 ~ 2013), and Chinese Biomedical (CBM) (1982 ~ 2013) databases were searched without language restrictions. Meta-analyses were conducted using Stata software (Version 12.0, Stata Corporation, College Station, TX, USA). Odds ratios (ORs) and their 95 % confidence intervals (95 %CIs) were calculated. Thirteen clinical case–control studies, which enrolled a total of 465 MM patients and 180 healthy subjects, were included in the meta-analysis. The results of our meta-analysis demonstrated that the frequencies of p15 INK4b and p16 INK4a promoter methylation in cancer samples were significantly higher than in normal samples ( p15 INK4b : OR = 6.26, 95 %CI = 3.87 ~ 10.12, P  < 0.001; p16 INK4a : OR = 2.26, 95 %CI = 1.22 ~ 4.20, P  < 0.001). Ethnicity-stratified analysis showed that the aberrant methylation of p15 INK4b was significantly related with the risk of MM among both Caucasians and Asians (all P  < 0.05). Furthermore, our results also illustrated a strong positive correlation between p16 INK4a promoter methylation and the pathogenesis of MM among Asians (OR = 5.17, 95 %CI = 3.45 ~ 7.74, P  < 0.001), but not among Caucasians ( P  > 0.05). The current meta-analysis confirms and reinforces existing findings that p15 INK4b and p16 INK4a promoter methylation may be closely implicated in the pathogenesis of MM.